Non-insulin-dependent diabetes mellitus and hypertriglyceridemia impair lipoprotein metabolism in chronic hemodialysis patients
Patients with diabetes mellitus undergoing chronic hemodialysis treatment have the worst outcome on dialysis due to an increased rate of cardiovascular complications. Nearly all patients present with dyslipidemia, a prominent vascular risk factor, probably responsible for the high rate of vascular i...
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| Veröffentlicht in: | Journal of the American Society of Nephrology 1999-02, Vol.10 (2), p.332-341 |
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| creator | QUASCHNING, T SCHÖMIG, M KELLER, M THIERY, J NAUCK, M SCHOLLMEYER, P WANNER, C KRÄMER-GUTH, A |
| description | Patients with diabetes mellitus undergoing chronic hemodialysis treatment have the worst outcome on dialysis due to an increased rate of cardiovascular complications. Nearly all patients present with dyslipidemia, a prominent vascular risk factor, probably responsible for the high rate of vascular injury. Since both uremia and diabetes predispose to hypertriglyceridemia, the present study was conducted to investigate the influence of diabetes mellitus and/or hypertriglyceridemia on lipoprotein metabolism in hemodialysis patients. LDL was isolated and characterized from hyper- and normotriglyceridemic diabetic and nondiabetic hemodialysis patients (n = 40; 10 in each group); also, LDL-receptor-dependent uptake and intracellular cholesterol metabolism were studied in HepG2 cells. In addition, scavenger-receptor-mediated uptake was examined in mouse peritoneal macrophages. LDL isolated from nondiabetic normotriglyceridemic hemodialysis patients exhibited impaired cellular uptake via the LDL receptor. Additionally, intracellular sterol synthesis was less inhibited and cholesterol esterification was reduced compared with LDL from healthy control subjects. Reduction of catabolic capacities was more marked in hemodialysis patients who were either diabetic or hypertriglyceridemic and even more pronounced in patients presenting with a combination of both diabetes and hypertriglyceridemia. Hypertriglyceridemic and diabetic patients showed reduced lipase activity and increased LDL oxidation. Furthermore, they accumulated a fraction of small, dense LDL, and LDL was predominantly taken up via the scavenger-receptor pathway in peritoneal macrophages. This study elucidates the distinct influence of diabetes and/or hypertriglyceridemia in hemodialysis patients on cellular LDL metabolism via specific and nonspecific metabolic pathways. Furthermore, it underscores the cumulative impact of these pathologic entities on impairment of lipoprotein metabolism and increase of cardiovascular risk. |
| doi_str_mv | 10.1681/ASN.V102332 |
| format | Article |
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Nearly all patients present with dyslipidemia, a prominent vascular risk factor, probably responsible for the high rate of vascular injury. Since both uremia and diabetes predispose to hypertriglyceridemia, the present study was conducted to investigate the influence of diabetes mellitus and/or hypertriglyceridemia on lipoprotein metabolism in hemodialysis patients. LDL was isolated and characterized from hyper- and normotriglyceridemic diabetic and nondiabetic hemodialysis patients (n = 40; 10 in each group); also, LDL-receptor-dependent uptake and intracellular cholesterol metabolism were studied in HepG2 cells. In addition, scavenger-receptor-mediated uptake was examined in mouse peritoneal macrophages. LDL isolated from nondiabetic normotriglyceridemic hemodialysis patients exhibited impaired cellular uptake via the LDL receptor. Additionally, intracellular sterol synthesis was less inhibited and cholesterol esterification was reduced compared with LDL from healthy control subjects. Reduction of catabolic capacities was more marked in hemodialysis patients who were either diabetic or hypertriglyceridemic and even more pronounced in patients presenting with a combination of both diabetes and hypertriglyceridemia. Hypertriglyceridemic and diabetic patients showed reduced lipase activity and increased LDL oxidation. Furthermore, they accumulated a fraction of small, dense LDL, and LDL was predominantly taken up via the scavenger-receptor pathway in peritoneal macrophages. This study elucidates the distinct influence of diabetes and/or hypertriglyceridemia in hemodialysis patients on cellular LDL metabolism via specific and nonspecific metabolic pathways. Furthermore, it underscores the cumulative impact of these pathologic entities on impairment of lipoprotein metabolism and increase of cardiovascular risk.</description><identifier>ISSN: 1046-6673</identifier><identifier>EISSN: 1533-3450</identifier><identifier>DOI: 10.1681/ASN.V102332</identifier><identifier>PMID: 10215333</identifier><identifier>CODEN: JASNEU</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Aged ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Apolipoproteins B - blood ; Biological and medical sciences ; Cholesterol Esters - biosynthesis ; Diabetes Mellitus, Type 2 - metabolism ; Emergency and intensive care: renal failure. Dialysis management ; Female ; Humans ; Hypertriglyceridemia - metabolism ; Intensive care medicine ; Lipase - blood ; Lipids - blood ; Lipids - classification ; Lipoproteins - metabolism ; Lipoproteins, LDL - blood ; Lipoproteins, LDL - chemistry ; Lipoproteins, LDL - metabolism ; Lipoproteins, LDL - pharmacology ; Liver - metabolism ; Male ; Medical sciences ; Mice ; Middle Aged ; Oxidation-Reduction ; Renal Dialysis ; Sterols - biosynthesis ; Time Factors ; Tumor Cells, Cultured</subject><ispartof>Journal of the American Society of Nephrology, 1999-02, Vol.10 (2), p.332-341</ispartof><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c351t-80232ba7103b77af66132184b5b6e79d1fd90f8818a9d25c38c409f29e9bf2293</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1698694$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10215333$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>QUASCHNING, T</creatorcontrib><creatorcontrib>SCHÖMIG, M</creatorcontrib><creatorcontrib>KELLER, M</creatorcontrib><creatorcontrib>THIERY, J</creatorcontrib><creatorcontrib>NAUCK, M</creatorcontrib><creatorcontrib>SCHOLLMEYER, P</creatorcontrib><creatorcontrib>WANNER, C</creatorcontrib><creatorcontrib>KRÄMER-GUTH, A</creatorcontrib><title>Non-insulin-dependent diabetes mellitus and hypertriglyceridemia impair lipoprotein metabolism in chronic hemodialysis patients</title><title>Journal of the American Society of Nephrology</title><addtitle>J Am Soc Nephrol</addtitle><description>Patients with diabetes mellitus undergoing chronic hemodialysis treatment have the worst outcome on dialysis due to an increased rate of cardiovascular complications. Nearly all patients present with dyslipidemia, a prominent vascular risk factor, probably responsible for the high rate of vascular injury. Since both uremia and diabetes predispose to hypertriglyceridemia, the present study was conducted to investigate the influence of diabetes mellitus and/or hypertriglyceridemia on lipoprotein metabolism in hemodialysis patients. LDL was isolated and characterized from hyper- and normotriglyceridemic diabetic and nondiabetic hemodialysis patients (n = 40; 10 in each group); also, LDL-receptor-dependent uptake and intracellular cholesterol metabolism were studied in HepG2 cells. In addition, scavenger-receptor-mediated uptake was examined in mouse peritoneal macrophages. LDL isolated from nondiabetic normotriglyceridemic hemodialysis patients exhibited impaired cellular uptake via the LDL receptor. Additionally, intracellular sterol synthesis was less inhibited and cholesterol esterification was reduced compared with LDL from healthy control subjects. Reduction of catabolic capacities was more marked in hemodialysis patients who were either diabetic or hypertriglyceridemic and even more pronounced in patients presenting with a combination of both diabetes and hypertriglyceridemia. Hypertriglyceridemic and diabetic patients showed reduced lipase activity and increased LDL oxidation. Furthermore, they accumulated a fraction of small, dense LDL, and LDL was predominantly taken up via the scavenger-receptor pathway in peritoneal macrophages. This study elucidates the distinct influence of diabetes and/or hypertriglyceridemia in hemodialysis patients on cellular LDL metabolism via specific and nonspecific metabolic pathways. Furthermore, it underscores the cumulative impact of these pathologic entities on impairment of lipoprotein metabolism and increase of cardiovascular risk.</description><subject>Aged</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Apolipoproteins B - blood</subject><subject>Biological and medical sciences</subject><subject>Cholesterol Esters - biosynthesis</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>Female</subject><subject>Humans</subject><subject>Hypertriglyceridemia - metabolism</subject><subject>Intensive care medicine</subject><subject>Lipase - blood</subject><subject>Lipids - blood</subject><subject>Lipids - classification</subject><subject>Lipoproteins - metabolism</subject><subject>Lipoproteins, LDL - blood</subject><subject>Lipoproteins, LDL - chemistry</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>Lipoproteins, LDL - pharmacology</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Middle Aged</subject><subject>Oxidation-Reduction</subject><subject>Renal Dialysis</subject><subject>Sterols - biosynthesis</subject><subject>Time Factors</subject><subject>Tumor Cells, Cultured</subject><issn>1046-6673</issn><issn>1533-3450</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpN0MuP1SAUBnBiNM5z5d6wMG4mHXm0UJaTia9kMi7U2TYUTr3HUFqBLu7Kf324uTfRFZD8-OB8hLzh7Jarnn-4-_54-8SZkFK8IOe8k7KRbcde1j1rVaOUlmfkIuffjPFOaP2anFV9cPKc_H1cYoMxbwFj42GF6CEW6tGOUCDTGULAsmVqo6e7_QqpJPwV9g4SepjRUpxXi4kGXJc1LQUw1kvFjkvAPNN6cru0RHR0B_NSc8M-Y6arLVgfylfk1WRDhuvTekl-fvr44_5L8_Dt89f7u4fGyY6Xpq_jidFqzuSotZ2U4lLwvh27UYE2nk_esKnveW-NF52TvWuZmYQBM05CGHlJ3h9z6x__bJDLMGN2dTgbYdnyoEynpdIHeHOELi05J5iGNeFs037gbDj0PdS-h1PfVb89xW7jDP4_eyy4gncnYLOzYUo2Osz_nDK9Mq18Bj91itk</recordid><startdate>19990201</startdate><enddate>19990201</enddate><creator>QUASCHNING, T</creator><creator>SCHÖMIG, M</creator><creator>KELLER, M</creator><creator>THIERY, J</creator><creator>NAUCK, M</creator><creator>SCHOLLMEYER, P</creator><creator>WANNER, C</creator><creator>KRÄMER-GUTH, A</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19990201</creationdate><title>Non-insulin-dependent diabetes mellitus and hypertriglyceridemia impair lipoprotein metabolism in chronic hemodialysis patients</title><author>QUASCHNING, T ; SCHÖMIG, M ; KELLER, M ; THIERY, J ; NAUCK, M ; SCHOLLMEYER, P ; WANNER, C ; KRÄMER-GUTH, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c351t-80232ba7103b77af66132184b5b6e79d1fd90f8818a9d25c38c409f29e9bf2293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Aged</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Apolipoproteins B - blood</topic><topic>Biological and medical sciences</topic><topic>Cholesterol Esters - biosynthesis</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Emergency and intensive care: renal failure. Dialysis management</topic><topic>Female</topic><topic>Humans</topic><topic>Hypertriglyceridemia - metabolism</topic><topic>Intensive care medicine</topic><topic>Lipase - blood</topic><topic>Lipids - blood</topic><topic>Lipids - classification</topic><topic>Lipoproteins - metabolism</topic><topic>Lipoproteins, LDL - blood</topic><topic>Lipoproteins, LDL - chemistry</topic><topic>Lipoproteins, LDL - metabolism</topic><topic>Lipoproteins, LDL - pharmacology</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Middle Aged</topic><topic>Oxidation-Reduction</topic><topic>Renal Dialysis</topic><topic>Sterols - biosynthesis</topic><topic>Time Factors</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>QUASCHNING, T</creatorcontrib><creatorcontrib>SCHÖMIG, M</creatorcontrib><creatorcontrib>KELLER, M</creatorcontrib><creatorcontrib>THIERY, J</creatorcontrib><creatorcontrib>NAUCK, M</creatorcontrib><creatorcontrib>SCHOLLMEYER, P</creatorcontrib><creatorcontrib>WANNER, C</creatorcontrib><creatorcontrib>KRÄMER-GUTH, A</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of the American Society of Nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>QUASCHNING, T</au><au>SCHÖMIG, M</au><au>KELLER, M</au><au>THIERY, J</au><au>NAUCK, M</au><au>SCHOLLMEYER, P</au><au>WANNER, C</au><au>KRÄMER-GUTH, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Non-insulin-dependent diabetes mellitus and hypertriglyceridemia impair lipoprotein metabolism in chronic hemodialysis patients</atitle><jtitle>Journal of the American Society of Nephrology</jtitle><addtitle>J Am Soc Nephrol</addtitle><date>1999-02-01</date><risdate>1999</risdate><volume>10</volume><issue>2</issue><spage>332</spage><epage>341</epage><pages>332-341</pages><issn>1046-6673</issn><eissn>1533-3450</eissn><coden>JASNEU</coden><abstract>Patients with diabetes mellitus undergoing chronic hemodialysis treatment have the worst outcome on dialysis due to an increased rate of cardiovascular complications. Nearly all patients present with dyslipidemia, a prominent vascular risk factor, probably responsible for the high rate of vascular injury. Since both uremia and diabetes predispose to hypertriglyceridemia, the present study was conducted to investigate the influence of diabetes mellitus and/or hypertriglyceridemia on lipoprotein metabolism in hemodialysis patients. LDL was isolated and characterized from hyper- and normotriglyceridemic diabetic and nondiabetic hemodialysis patients (n = 40; 10 in each group); also, LDL-receptor-dependent uptake and intracellular cholesterol metabolism were studied in HepG2 cells. In addition, scavenger-receptor-mediated uptake was examined in mouse peritoneal macrophages. LDL isolated from nondiabetic normotriglyceridemic hemodialysis patients exhibited impaired cellular uptake via the LDL receptor. Additionally, intracellular sterol synthesis was less inhibited and cholesterol esterification was reduced compared with LDL from healthy control subjects. Reduction of catabolic capacities was more marked in hemodialysis patients who were either diabetic or hypertriglyceridemic and even more pronounced in patients presenting with a combination of both diabetes and hypertriglyceridemia. Hypertriglyceridemic and diabetic patients showed reduced lipase activity and increased LDL oxidation. Furthermore, they accumulated a fraction of small, dense LDL, and LDL was predominantly taken up via the scavenger-receptor pathway in peritoneal macrophages. This study elucidates the distinct influence of diabetes and/or hypertriglyceridemia in hemodialysis patients on cellular LDL metabolism via specific and nonspecific metabolic pathways. Furthermore, it underscores the cumulative impact of these pathologic entities on impairment of lipoprotein metabolism and increase of cardiovascular risk.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>10215333</pmid><doi>10.1681/ASN.V102332</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Apolipoproteins B - blood Biological and medical sciences Cholesterol Esters - biosynthesis Diabetes Mellitus, Type 2 - metabolism Emergency and intensive care: renal failure. Dialysis management Female Humans Hypertriglyceridemia - metabolism Intensive care medicine Lipase - blood Lipids - blood Lipids - classification Lipoproteins - metabolism Lipoproteins, LDL - blood Lipoproteins, LDL - chemistry Lipoproteins, LDL - metabolism Lipoproteins, LDL - pharmacology Liver - metabolism Male Medical sciences Mice Middle Aged Oxidation-Reduction Renal Dialysis Sterols - biosynthesis Time Factors Tumor Cells, Cultured |
| title | Non-insulin-dependent diabetes mellitus and hypertriglyceridemia impair lipoprotein metabolism in chronic hemodialysis patients |
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